NF.KAPPA.B-p65 Dependent Transcriptional Regulation of Glycosyltransferases in Human Colon Adenocarcinoma HT-29 by Stimulation with Tumor Necrosis Factor .ALPHA.

Higai, Koji; Ishihara, Saki; Matsumoto, Kojiro

doi:10.1248/bpb.29.2372

Cited by 35 publications

(22 citation statements)

References 23 publications

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“…In the hepatocellular carcinoma HuH-7 cells, IL-1β has been reported to enhance the expression of FUT6 and ST3GalIV inducing the synthesis of sialyl-Lewis x [38]; and in colon cancer cells, Immunohistochemical detection of sialyl-Lewis x. Decreased levels of s Le x were detected in IL-1β and IL-6 treated mice compared to control tumors TNF-α treatment activates the NF-κB pathway associated to the expression of p65 transcription factor and promotes biphasic and transient increases in the transcription levels of several glycosyltransferases among them FUT4 [30]. Also, it has been described that treatments of bronchial mucosa explants with IL-6 and IL-8 induce a significant increase in the expression of specific fucosyltranferases, FUT3 and FUT11, sialyltransferases, ST3GalVI and ST6GalII, and sulfotransferases, CHST4 and CHST6, implicated in the biosynthesis of sialyl-Lewis x and 6-sulfo-sialyl-Lewis x [39].…”

Section: Discussionmentioning

confidence: 99%

“…After rDNAse I (Ambion) treatment, mRNA levels of FUT1, FUT2, FUT3, FUT4, FUT5, ST3GalIII, and ST3GalIV, were quantified in triplicate using QuantiTect SYBR green RT-PCR (Qiagen). The primers used for amplification of FUT1, FUT2, FUT3 and FUT4 were described by Higai [30], FUT5 primers were: F: 5′-TGGGTGTGACCTCGGCGTGA-3′, and R: 5′-AAACCAG CCTGCACCATCGCC-3′, ST3Gal III primers were: F: 5′-GGTGGCAGTCGCAGTCGGCAGGATTT-3′, and R: 5′-CATGCGAACGGTCTCATAGTAGTG-3′, and ST3GalIV primers were: F: 5′-CGGGTGCGAAAGGGTTT-3′ and R: 5′-GGGCTCCGAGACCTGAGGGG-3′. Hypoxanthineguanine phosphoribosyl transferase (HPRT) mRNA (GeneCardsdatabase, NCBI36:X) was analyzed as an internal control.…”

Section: Rna Extraction and Quantitative Rt-pcrmentioning

confidence: 99%

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Regulation of glycosyltransferases and Lewis antigens expression by IL-1β and IL-6 in human gastric cancer cells

et al. 2011

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Inflammation of stomach mucosa has been postulated as initiator of gastric carcinogenesis and the presence of pro-inflammatory cytokines can regulate specific genes involved in this process. The cellular expression pattern of glycosyltransferases and Lewis antigens detected in the normal mucosa changed during the neoplassic transformation. The aim of this work was to determine the regulation of specific fucosyltransferases and sialyltransferases by IL-1β and IL-6 pro-inflammatory cytokines in MKN45 gastric cancer cells. IL-1β induced significant increases in the mRNA levels of FUT1, FUT2 and FUT4, and decreases of FUT3 and FUT5. In IL-6 treatments, enhanced FUT1 and lower FUT3 and FUT5 mRNA expression were detected. No substantial changes were observed in the levels of ST3GalIII and ST3GalIV. The activation of FUT1, FUT2 and FUT4 by IL-1β is through the NF-κB pathway and the down-regulation of FUT3 and FUT5 by IL-6 is through the gp130/STAT-3 pathway, since they are inhibited specifically by panepoxydone and AG490, respectively. The levels of Lewis antigens after IL-1β or IL-6 stimulation decreased for sialyl-Lewis x, and no significant differences were found in the rest of the Lewis antigens analyzed, as it was also observed in subcutaneous mice tumors from MKN45 cells treated with IL-1β or IL-6. In addition, in 61 human intestinal-type gastric tumors, sialyl-Lewis x was highly detected in samples from patients that developed metastasis. These results indicate that the expression of the fucosyltransferases involved in the synthesis of Lewis antigens in gastric cancer cells can be specifically modulated by IL-1β and IL-6 inflammatory cytokines.

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Section: Discussionmentioning

confidence: 99%

Section: Rna Extraction and Quantitative Rt-pcrmentioning

confidence: 99%

Regulation of glycosyltransferases and Lewis antigens expression by IL-1β and IL-6 in human gastric cancer cells

et al. 2011

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“…Both the COX-2 and TFNα promoters contain NF-kBp50/p65 binding sites and are responsive to transcriptional up-regulation via this pro-inflammatory transcription factor [5,18,25]. The neuroprotective mechanism of BUDeR, and LAU-0901 against this multitude of pathogenic PAF actions are not completely understood, however each have been shown to impede some aspect of NF-kBp50/p65-mediated gene up-regulation [13][14][15][16].…”

Section: Discussionmentioning

confidence: 99%

Synergism in the repression of COX-2- and TNFα-induction in platelet activating factor-stressed human neural cells

Boetkjaer

Boedker

Zhao

et al. 2007

Neuroscience Letters

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Platelet activating factor (PAF; β-acetyl-γ-O-hexadecyl-L-α-phosphatidylcholine) triggers a rapid pro-inflammatory gene expression program in primary cultures of human neural (HN) cells. Two genes and gene products consistently induced after PAF treatment are the cytosoluble prostaglandin synthase cycloooxygenase-2 (COX-2) and the pro-apoptotic tumor necrosis factor alpha (TNFα). Both of these mediators are associated with the activation of inflammatory signaling, neural cell dysfunction, apoptosis and brain cell death, and both have been found to be up-regulated after brain injury in vivo. In this study we investigated the effects of the non-halogenated synthetic glucocorticoid budesonide epimer R (BUDeR), the novel PAF antagonist LAU-0901, and the electron spin trap and free radical scavenger phenyl butyl nitrone (PBN), upon early COX-2 and TNFα gene activation and prostaglandin E 2 (PGE 2 ) release in PAF-stressed primary HN cells. The data indicate that these three biochemically unrelated classes of inflammatory repressors act synergistically in modulating PAF-induced up-regulation of COX-2, TNFα, and PGE 2 by quenching oxidative stress or inflammatory signaling, resulting in increased HN cell survival. These, or analogous classes of compounds, may be useful in the design of more effective combinatorial pharmacotherapeutic strategies in the treatment of complex neuro-inflammatory disorders.

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“…However, mutational studies confirm that other factors must play a role (40). In porcine kidney cells, transcriptional activation of this sialyltransferase can be induced by TGF-␤1 (41), and in the colon carci- noma cell line HT-29, tumor necrosis factor ␣ can enhance ST3Gal-I expression through NFB binding sites (31). We now show that increased expression of ST3Gal-I in breast cancer cells can be induced by COX-2 working through the prostanoid PGE2.…”

Section: Discussionmentioning

confidence: 99%

Cyclooxygenase-2 Enzyme Induces the Expression of the -2,3-Sialyltransferase-3 (ST3Gal-I) in Breast Cancer

Sproviero

Julien

Burford

et al. 2012

Journal of Biological Chemistry

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NF.KAPPA.B-p65 Dependent Transcriptional Regulation of Glycosyltransferases in Human Colon Adenocarcinoma HT-29 by Stimulation with Tumor Necrosis Factor .ALPHA.

Cited by 35 publications

References 23 publications

Regulation of glycosyltransferases and Lewis antigens expression by IL-1β and IL-6 in human gastric cancer cells

Regulation of glycosyltransferases and Lewis antigens expression by IL-1β and IL-6 in human gastric cancer cells

Synergism in the repression of COX-2- and TNFα-induction in platelet activating factor-stressed human neural cells

Cyclooxygenase-2 Enzyme Induces the Expression of the -2,3-Sialyltransferase-3 (ST3Gal-I) in Breast Cancer

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